Eye involvement occurs in about 10–90% of cases. Manifestations in the eye include uveitis, uveoparotitis, and retinal inflammation, which may result in loss of visual acuity or blindness. The most common ophthalmologic manifestation of sarcoidosis is uveitis. The combination of anterior uveitis, parotitis, VII cranial nerve paralysis and fever is called uveoparotid fever or Heerfordt syndrome (). Development of scleral nodule associated with sarcoidosis has been observed.

Any of the components of the nervous system can be involved. Sarcoidosis affecting the nervous system is known as neurosarcoidosis. Cranial nerves are most commonly affected, accounting for about 5–30% of neurosarcoidosis cases, and peripheral facial nerve palsy, often bilateral, is the most common neurological manifestation of sarcoidosis. It occurs suddenly and is usually transient. The central nervous system involvement is present in 10–25% of sarcoidosis cases. Other common manifestations of neurosarcoidosis include optic nerve dysfunction, papilledema, palate dysfunction, neuroendocrine changes, hearing abnormalities, hypothalamic and pituitary abnormalities, chronic meningitis, and peripheral neuropathy. Myelopathy, that is spinal cord involvement, occurs in about 16–43% of neurosarcoidosis cases and is often associated with the poorest prognosis of the neurosarcoidosis subtypes. Whereas facial nerve palsies and acute meningitis due to sarcoidosis tends to have the most favourable prognosis. Another common finding in sarcoidosis with neurological involvement is autonomic or sensory small fiber neuropathy. Neuroendocrine sarcoidosis accounts for about 5–10% of neurosarcoidosis cases and can lead to diabetes insipidus, changes in menstrual cycle and hypothalamic dysfunction. The latter can lead to changes in body temperature, mood and prolactin (see the endocrine and exocrine section for details).

Common signs and symptoms of intestinal cryptosporidiosis include:

- Moderate to severe watery diarrhea, sometimes contains mucus and rarely contains blood or leukocytes

- In very severe cases, diarrhea may be profuse and cholera-like with malabsorption and hypovolemia

- Low-grade fever

- Crampy abdominal pain

- Dehydration

- Weight loss

- Fatigue

- Nausea and vomiting – suggests upper GI tract involvement and may lead to respiratory cryptosporidiosis

- Epigastric or right upper quadrant tenderness

Less common or rare signs and symptoms include:

- Reactive arthritis (may affect the hands, knees, ankles, and feet)

- Jaundice – suggests hepatobiliary involvement

- Ascites – suggests pancreatic involvement

The human disease occurs in two stages: an acute stage, which occurs shortly after an initial infection, and a chronic stage that develops over many years.

The acute phase lasts for the first few weeks or months of infection. It usually occurs unnoticed because it is symptom-free or exhibits only mild symptoms that are not unique to Chagas disease. These can include fever, fatigue, body aches, muscle pain, headache, rash, loss of appetite, diarrhea, nausea, and vomiting. The signs on physical examination can include mild enlargement of the liver or spleen, swollen glands, and local swelling (a chagoma) where the parasite entered the body.

The most recognized marker of acute Chagas disease is called Romaña's sign, which includes swelling of the eyelids on the side of the face near the bite wound or where the bug feces were deposited or accidentally rubbed into the eye. Rarely, young children, or adults may die from the acute disease due to severe inflammation/infection of the heart muscle (myocarditis) or brain (meningoencephalitis). The acute phase also can be severe in people with weakened immune systems.

If symptoms develop during the acute phase, they usually resolve spontaneously within three to eight weeks in approximately 90% of individuals. Although the symptoms resolve, even with treatment the infection persists and enters a chronic phase. Of individuals with chronic Chagas disease, 60–80% will never develop symptoms (called "indeterminate" chronic Chagas disease), while the remaining 20–40% will develop life-threatening heart and/or digestive disorders during their lifetime (called "determinate" chronic Chagas disease). In 10% of individuals, the disease progresses directly from the acute form to a symptomatic clinical form of chronic Chagas disease.

The symptomatic (determinate) chronic stage affects the nervous system, digestive system and heart. About two-thirds of people with chronic symptoms have cardiac damage, including dilated cardiomyopathy, which causes heart rhythm abnormalities and may result in sudden death. About one-third of patients go on to develop digestive system damage, resulting in dilation of the digestive tract (megacolon and megaesophagus), accompanied by severe weight loss. Swallowing difficulties (secondary achalasia) may be the first symptom of digestive disturbances and may lead to malnutrition.

20% to 50% of individuals with intestinal involvement also exhibit cardiac involvement. Up to 10% of chronically infected individuals develop neuritis that results in altered tendon reflexes and sensory impairment. Isolated cases exhibit central nervous system involvement, including dementia, confusion, chronic encephalopathy and sensory and motor deficits.

The clinical manifestations of Chagas disease are due to cell death in the target tissues that occurs during the infective cycle, by sequentially inducing an inflammatory response, cellular lesions, and fibrosis. For example, intracellular amastigotes destroy the intramural neurons of the autonomic nervous system in the intestine and heart, leading to megaintestine and heart aneurysms, respectively. If left untreated, Chagas disease can be fatal, in most cases due to heart muscle damage.

Researchers have published conflicting reports concerning whether "Blastocystis" causes symptoms in humans, with one of the earliest reports in 1916. The incidence of reports associated with symptoms began to increase in 1984, with physicians from Saudi Arabia reporting symptoms in humans and US physicians reporting symptoms in individuals with travel to less developed countries. A lively debate ensued in the early 1990s, with some physicians objecting to publication of reports that "Blastocystis" caused disease. Some researchers believe the debate has been resolved by finding of multiple species of "Blastocystis" that can infect humans, with some causing symptoms and others being harmless (see Genetics and Symptoms).

A few of most commonly reported symptoms are:

- abdominal pain

- itching, usually anal itching

- constipation

- diarrhea

- watery or loose stools

- weight loss

- fatigue

- flatulence

Some less commonly reported symptoms include:

- Skin rash

- Headache, depression

- Arthritic symptoms and joint pain

- Intestinal inflammation

Symptoms of upper respiratory cryptosporidiosis include:

- Inflammation of the nasal mucosa, sinuses, larynx, or trachea

- Nasal discharge

- Voice change (e.g., hoarseness)

Symptoms of lower respiratory cryptosporidiosis include:

- Cough

- Shortness of breath

- Fever

- Hypoxemia

Dracunculiasis is diagnosed by seeing the worms emerging from the lesions on the legs of infected individuals and by microscopic examinations of the larvae.

As the worm moves downwards, usually to the lower leg, through the subcutaneous tissues, it leads to intense pain localized to its path of travel. The burning sensation experienced by infected people has led to the disease being called "the fiery serpent". Other symptoms include fever, nausea, and vomiting. Female worms cause allergic reactions during blister formation as they migrate to the skin, causing an intense burning pain. Such allergic reactions produce rashes, nausea, diarrhea, dizziness, and localized edema. When the blister bursts, allergic reactions subside, but skin ulcers form, through which the worm can protrude. Only when the worm is removed is healing complete. Death of adult worms in joints can lead to arthritis and paralysis in the spinal cord.

Blastomycosis can present in one of the following ways:

- a flu-like illness with fever, chills, arthralgia (joint pain), myalgia (muscle pain), headache, and a nonproductive cough which resolves within days.

- an acute illness resembling bacterial pneumonia, with symptoms of high fever, chills, a productive cough, and pleuritic chest pain.

- a chronic illness that mimics tuberculosis or lung cancer, with symptoms of low-grade fever, a productive cough, night sweats, and weight loss.

- a fast, progressive, and severe disease that manifests as ARDS, with fever, shortness of breath, tachypnea, hypoxemia, and diffuse pulmonary infiltrates.

- skin lesions, usually asymptomatic, can be verrucous (wart-like) or ulcerated with small pustules at the margins.

- bone lytic lesions can cause bone or joint pain.

- prostatitis may be asymptomatic or may cause pain on urinating.

- laryngeal involvement causes hoarseness.

- 40% immunocompromised individuals have CNS involvement and present as brain abscess, epidural abscess or meningitis.

The onset of paralysis (spastic paraparesis) is sudden and symmetrical and affects the legs more than the arms. The resulting disability is permanent but does not progress. Typically, a patient is standing and walking on the balls of the feet with rigid legs and often with ankle clonus.

Initially, most patients experience generalized weakness during the first days and are bedridden for some days or weeks before trying to walk. Occasional blurred vision and/or speech difficulties typically clear during the first month, except in severely affected patients. Spasticity is present from the first day, without any initial phase of flaccidity. After the initial weeks of functional improvement, the spastic paraparesis remains stable for the rest of life. Some patients may suffer an abrupt aggravating episode, e.g. a sudden and permanent worsening of the spastic paraparesis. Such episodes are identical to the initial onset and can therefore be interpreted as a "second onset".

The severity of konzo varies; cases range from only hyperreflexia in the lower limbs to a severely disabled, bedridden patient with spastic paraparesis, associated weakness of the trunk and arms, impaired eye movements, speech and possibly visual impairment. Although the severity varies from patient to patient, the longest upper motor neurons are invariably more affected than the shorter ones. Thus, a konzo patient with speech impairment always shows severe symptoms in the legs and arms.

Recently, neuropsychological effects of konzo have been described from DR Congo.

In humans, after an incubation period of 5–19 days, the symptoms of the disease range from inapparent illness to systemic illness with severe pneumonia. It presents chiefly as an atypical pneumonia. In the first week of psittacosis the symptoms mimic typhoid fever: prostrating high fevers, joint pains, diarrhea, conjunctivitis, nose bleeds and low level of white blood cells in the blood. Rose spots can appear and these are called Horder's spots. Spleen enlargement is common towards the end of the first week. It may become a serious lung infection. Diagnosis can be suspected in case of respiratory infection associated with splenomegaly and/or epistaxis. Headache can be so severe that it suggests meningitis and some nuchal rigidity is not unusual. Towards the end of the first week stupor or even coma can result in severe cases.

The second week is more akin to acute bacteremic pneumococcal pneumonia with continuous high fevers, headaches, cough, and dyspnea. X-rays show patchy infiltrates or a diffuse whiteout of lung fields.

Complications in the form of endocarditis, liver inflammation, inflammation of the heart's muscle, joint inflammation, keratoconjunctivitis (occasionally extranodal marginal zone lymphoma of the lacrimal gland/orbit), and neurologic complications (brain inflammation) may occasionally occur. Severe pneumonia requiring intensive-care support may also occur. Fatal cases have been reported (less than 1% of cases).

The average age of onset is the early to mid 30s. Exertional dyspnea and spontaneous pneumothorax have been reported as the initial presentation of the disease in 49% and 46% of patients, respectively.

Diagnosis is typically delayed 5 to 6 years. The condition is often misdiagnosed as asthma or chronic obstructive pulmonary disease. The first pneumothorax precedes the diagnosis of LAM in 82% of patients. The consensus clinical definition of LAM includes multiple symptoms:

- Fatigue

- Cough

- Hemoptysis (rarely massive)

- Chest pain

- Chylous complications arising from lymphatic obstruction, including

- Chylothorax

- Chylous ascites

- Chylopericaridium

- Chyloptysis

- Chyluria

- Chyle in vaginal discharge

- Chyle in stool.

- Angiomyolipomas (fatty kidney tumors) are present in about 30% of patients with sporadic LAM and up to 90% of patients with TSC-LAM. Angiomyolipomas can sometimes spontaneously bleed, causing pain or hypotension.

- Cystic lymphangiomas or lymph nodes with hypodense centers, which mimic necrotizing lymphomas, ovarian or renal cancers, or other malignancies can occur in the retroperitoneum, pelvis or mediastinum.

Lung destruction in LAM is a consequence of diffuse infiltration by neoplastic smooth muscle-like cells that invade all lung structures including the lymphatics, airway walls, blood vessels and interstitial spaces. The consequences of vessel and airway obstruction include chylous fluid accumulations, hemoptysis, airflow obstruction and pneumothorax. The typical disease course displays progressive dyspnea on exertion, spaced by recurrent pneumothoraces and in some patients, chylous pleural effusions or ascites.

Most people have dyspnea on exertion with daily activities by 10 years after symptom onset. Many patients require supplemental oxygen over that interval.

Half of all children and a quarter of previously healthy adults are asymptomatic with "Babesia" infection. When people do develop symptoms, the most common are fever and hemolytic anemia, symptoms that are similar to those of malaria. People with symptoms usually become ill 1 to 4 weeks after the bite, or 1 to 9 weeks after transfusion of contaminated blood products. A person infected with babesiosis gradually develops malaise and fatigue, followed by a fever. Hemolytic anemia, in which red blood cells are destroyed and removed from the blood, also develops. Chills, sweats, and thrombocytopenia are also common symptoms. Symptoms may last from several days to several months.

Less common symptoms and physical exam findings of mild-to-moderate babesiosis:

In more severe cases, symptoms similar to malaria occur, with fevers up to 40.5 °C (105 °F), shaking chills, and severe anemia (hemolytic anemia). Organ failure may follow, including adult respiratory distress syndrome. Severe cases occur mostly in people who have had a splenectomy. Severe cases are also more likely to occur in the very young, very old, and persons with immunodeficiency, such as HIV/AIDS patients.

A reported increase in human babesiosis diagnoses in the 2000s is thought to be caused by more widespread testing and higher numbers of people with immunodeficiencies coming in contact with ticks, the disease vector. Little is known about the occurrence of "Babesia" species in malaria-endemic areas, where "Babesia" can easily be misdiagnosed as "Plasmodium". Human patients with repeat babesiosis infection may exhibit premunity.

Dracunculiasis, also called Guinea-worm disease (GWD), is an infection by the Guinea worm. A person becomes infected when they drink water that contains water fleas infected with guinea worm larvae. Initially there are no symptoms. About one year later, the person develops a painful burning feeling as the female worm forms a blister in the skin, usually on a lower limb. The worm then emerges from the skin over the course of a few weeks. During this time, it may be difficult to walk or work. It is very uncommon for the disease to cause death.

In humans, the only known cause is "Dracunculus medinensis". The worm is about one to two millimeters wide, and an adult female is 60 to 100 centimeters long (males are much shorter at ). Outside of humans, the young form can survive up to three weeks, during which they must be eaten by water fleas to continue to develop. The larva inside water fleas may survive up to four months. Thus, in order for the disease to remain in an area, it must occur each year in humans. A diagnosis of the disease can usually be made based on the signs and symptoms.

Prevention is by early diagnosis of the disease followed by keeping the person from putting the wound in drinking water to decrease spread of the parasite. Other efforts include improving access to clean water and otherwise filtering water if it is not clean. Filtering through a cloth is often enough. Contaminated drinking water may be treated with a chemical called temefos to kill the larva. There is no medication or vaccine against the disease. The worm may be slowly removed over a few weeks by rolling it over a stick. The ulcers formed by the emerging worm may get infected by bacteria. Pain may continue for months after the worm has been removed.

In 2015 there were 22 reported cases of the disease while in 2016 there were 25. This is down from an estimated 3.5 million cases in 1986. In 2016 the disease occurred in three countries, all in Africa, down from 20 countries in the 1980s. It will likely be the first parasitic disease to be globally eradicated. Guinea worm disease has been known since ancient times. The method of removing the worm is described in the Egyptian medical Ebers Papyrus, dating from 1550 BC. The name dracunculiasis is derived from the Latin "affliction with little dragons", while the name "guinea worm" appeared after Europeans saw the disease on the Guinea coast of West Africa in the 17th century. Other "Dracunculus" species are known to infect various mammals, but do not appear to infect humans. Dracunculiasis is classified as a neglected tropical disease. Because dogs may also become infected, the eradication program is monitoring and treating dogs as well.

Chagas disease, also known as American trypanosomiasis, is a tropical parasitic disease caused by the protist "Trypanosoma cruzi". It is spread mostly by insects known as Triatominae, or "kissing bugs". The symptoms change over the course of the infection. In the early stage, symptoms are typically either not present or mild, and may include fever, swollen lymph nodes, headaches, or local swelling at the site of the bite. After 8–12 weeks, individuals enter the chronic phase of disease and in 60–70% it never produces further symptoms. The other 30 to 40% of people develop further symptoms 10 to 30 years after the initial infection, including enlargement of the ventricles of the heart in 20 to 30%, leading to heart failure. An enlarged esophagus or an enlarged colon may also occur in 10% of people.

"T. cruzi" is commonly spread to humans and other mammals by the blood-sucking "kissing bugs" of the subfamily Triatominae. These insects are known by a number of local names, including: "vinchuca" in Argentina, Bolivia, Chile and Paraguay, "barbeiro" (the barber) in Brazil, "pito" in Colombia, "chinche" in Central America, and "chipo" in Venezuela. The disease may also be spread through blood transfusion, organ transplantation, eating food contaminated with the parasites, and by vertical transmission (from a mother to her fetus). Diagnosis of early disease is by finding the parasite in the blood using a microscope. Chronic disease is diagnosed by finding antibodies for "T. cruzi" in the blood.

Prevention mostly involves eliminating kissing bugs and avoiding their bites. Other preventive efforts include screening blood used for transfusions. A vaccine has not been developed as of 2017. Early infections are treatable with the medication benznidazole or nifurtimox. Medication nearly always results in a cure if given early, but becomes less effective the longer a person has had Chagas disease. When used in chronic disease, medication may delay or prevent the development of end–stage symptoms. Benznidazole and nifurtimox cause temporary side effects in up to 40% of people including skin disorders, brain toxicity, and digestive system irritation.

It is estimated that 6.6 million people, mostly in Mexico, Central America and South America, have Chagas disease as of 2015. In 2015, Chagas was estimated to result in 8,000 deaths. Most people with the disease are poor, and most do not realize they are infected. Large-scale population movements have increased the areas where Chagas disease is found and these include many European countries and the United States. These areas have also seen an increase in the years up to 2014. The disease was first described in 1909 by the Brazilian physician Carlos Chagas, after whom it is named. Chagas disease is classified as a neglected tropical disease. It affects more than 150 other animals.

The course of fasciolosis in humans has 4 main phases:

- Incubation phase: from the ingestion of metacercariae to the appearance of the first symptoms; time period: few days to 3 months; depends on number of ingested metacercariae and immune status of host

- Invasive or acute phase: fluke migration up to the bile ducts. This phase is a result of mechanical destruction of the hepatic tissue and the peritoneum by migrating juvenile flukes causing localized and or generalized toxic and allergic reactions. The major symptoms of this phase are:

- Fever: usually the first symptom of the disease;

- Abdominal pain

- Gastrointestinal disturbances: loss of appetite, flatulence, nausea, diarrhea

- Urticaria

- Respiratory symptoms (very rare): cough, dyspnoea, chest pain, hemoptysis

- Hepatomegaly and splenomegaly

- Ascites

- Anaemia

- Jaundice

- Latent phase: This phase can last for months or years. The proportion of asymptomatic subjects in this phase is unknown. They are often discovered during family screening after a patient is diagnosed.

- Chronic or obstructive phase:

This phase may develop months or years after initial infection. Adult flukes in the bile ducts cause inflammation and hyperplasia of the epithelium. The resulting cholangitis and cholecystitis, combined with the large body of the flukes, are sufficient to cause mechanical obstruction of the biliary duct. In this phase, biliary colic, epigastric pain, fatty food intolerance, nausea, jaundice, pruritus, right upper-quadrant abdominal tenderness, etc., are clinical manifestations indistinguishable from cholangitis, cholecystitis and cholelithiasis of other origins. Hepatic enlargement may be associated with an enlarged spleen or ascites. In case of obstruction, the gall bladder is usually enlarged and edematous with thickening of the wall (Ref: Hepatobiliary Fascioliasis:

Sonographic and CT Findings in 87 Patients During the InitialPhase and Long-Term Follow-Up. Adnan Kabaalioglu, Kagan Ceken, Emel Alimoglu, Rabin Saba, Metin Cubuk, Gokhan Arslan, Ali Apaydin. AJR 2007; 189:824–828). Fibrous adhesions of the gall bladder to adjacent organs are common. Lithiasis of the bile duct or gall bladder is frequent and the stones are usually small and multiple.

On post-mortem examination (necropsy), the most obvious gross lesion is subcutaneous oedema in the submandibular and pectoral (brisket) regions. Petechial haemorrhages are found subcutaneously and in the thoracic cavity. In addition, congestion and various degrees of consolidation of the lung may occur. Animals that die within 24–36 hours, have only few petechial haemorrhages on the heart and generalised congestion of the lung, while in animals that die after 72 hours, petechial and ecchymotic haemorrhages were more evident and lung consolidation are more extensive.

Mesoamerican nephropathy (MeN) is a currently unexplained epidemic of chronic kidney disease of unknown origin (CKDu), prevalent in the Pacific Ocean coastal low lands of the Mesoamerican region, including southern Mexico, Guatemala, El Salvador, Nicaragua, Honduras and Costa Rica. In rural areas of Nicaragua the disease is colloquially called creatinina.

This CKD epidemic in Central America spans along a nearly 1000 kilometer stretch of the Pacific coast. In El Salvador and Nicaragua alone, the reported number of men dying from this painful disease has risen five-fold in the last 20 years, although some researchers believe hidden cases have always been there and this increment in official data could be partially due to the recent increase in reports and improved case search, pushed by the growing social and political interest in the disease. In El Salvador, the disease has become the second leading cause of death among adult men, and according to a recent editorial, it has been estimated that this largely unknown epidemic has caused the premature death of at least 20,000 men in the region. Science Magazine reports: "In El Salvador alone, PAHO's latest figures say CKD of all causes kills at least 2,500 people in the country each year".

The people affected by the epidemic are mainly young and middle-aged male laborers in the agricultural sector, particularly sugarcane workers. The disease has also been found to be prevalent in other occupations with a high risk of heat stress, implying strenuous work (miners, construction, port and transportation workers) in the high temperatures of the coastlands. The epidemic appears to affect particular Pacific coastal regions of Nicaragua, El Salvador, Costa Rica, and Guatemala.

Lymphangioleiomyomatosis (LAM) is a rare, progressive and systemic disease that typically results in cystic lung destruction. It predominantly affects women, especially during childbearing years.

In rabbits of the genus "Sylvilagus" (cottontail rabbits) living in the Americas, myxomatosis causes only localized skin tumors, but the European rabbit ("Oryctolagus cuniculus") is more severely affected. At first, normally the disease is visible by lumps (myxomata) and puffiness around the head and genitals. It may progress to acute conjunctivitis and possibly blindness; however, this also may be the first visible symptom of the disease. The rabbits become listless, lose appetite, and develop a fever. Secondary bacterial infections occur in most cases, which cause pneumonia and purulent inflammation of the lungs. In cases where the rabbit has little or no resistance, death may take place rapidly, often in as little as 48 hours; most cases result in death within 14 days. Often the symptoms like blindness make the infected rabbit more vulnerable to predators.

Psittacosis—also known as parrot fever, and ornithosis—is a zoonotic infectious disease caused by a bacterium called "Chlamydia psittaci" and contracted from infected parrots, such as macaws, cockatiels and budgerigars, and pigeons, sparrows, ducks, hens, gulls and many other species of bird. The incidence of infection in canaries and finches is believed to be lower than in psittacine birds.

In certain contexts, the word is used when the disease is carried by any species of bird belonging to the family Psittacidae, whereas "ornithosis" is used when other birds carry the disease.

A wide variety of clinical signs have been described for HS in cattle and buffaloes. The incubation periods (the time between exposure and observable disease) for buffalo calves 4–10 months of age varies according to the route of infection. The incubation period is 12–14 hours, approximately 30 hours and 46–80 hours for subcutaneous infection, oral infection and natural exposure, respectively.

There is variability in the duration of the clinical course of the disease. In the case of experimental subcutaneous infection, the clinical course lasted only a few hours, while it persisted for 2–5 days following oral infection and in buffaloes and cattle that had been exposed to naturally-infected animals. It has also been recorded from field observations that the clinical courses of per-acute and acute cases were 4–12 hours and 2–3 days, respectively.

Generally, progression of the disease in buffaloes and cattle is divided into three phases. Phase one is characterised by fever, with a rectal temperature of , loss of appetite and depression. Phase two is typified by increased respiration rate (40–50/minute), laboured breathing, clear nasal discharge (turns opaque and mucopurulent as the disease progresses), salivation and submandibular oedema spreading to the pectoral (brisket) region and even to the forelegs. Finally, in phase three, there is typically recumbency, continued acute respiratory distress and terminal septicaemia. The three phases overlap when the disease course is short. In general, buffaloes have a more acute onset of disease than cattle, with a shorter duration.

These most often occur years after the development of ptosis and ophthalmoplegia. Atrioventricular(abbreviated "AV") block is the most common cardiac conduction deficit. This often progresses to a Third-degree atrioventricular block, which is a complete blockage of the electrical conduction from the atrium to the ventricle. Symptoms of heart block include syncope, exercise intolerance, and bradycardia

Blastocystosis refers to a medical condition caused by infection with "Blastocystis". "Blastocystis" is a protozoal, single-celled parasite that inhabits the gastrointestinal tracts of humans and other animals. Many different types of "Blastocystis" exist, and they can infect humans, farm animals, birds, rodents, amphibians, reptiles, fish, and even cockroaches. Blastocystosis has been found to be a possible risk factor for development of IBS (Irritable Bowel Syndrome).

The WHO has recommended three criteria for the diagnosis of konzo:

- a visible symmetric spastic abnormality of gait while walking or running;

- a history of onset of less than one week followed by a non-progressive course in a formerly healthy person;

- bilaterally exaggerated knee or ankle jerk reflexes without signs of disease of the spine.

Depending on its severity, konzo is divided into three categories: mild when individuals are able to walk without support, moderate when individuals need one or two sticks to walk, and severe when the affected person is unable to walk unsupported.

The cause of MeN is unclear, but it is certainly not explained by conventional causes such as diabetes mellitus or hypertension. Many risk factors have been proposed but to date, the causes of the disease remain uncertain and controversial.